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Calcitriol inhibits the growth of MHCC97 heptocellular cell lines by down‐modulating c‐met and ERK expressions
Author(s) -
Wu Fusheng,
Zheng Shusen,
Wu Lingjiao,
Teng Lisong,
Ma Zhimin,
Zhao Wenhe,
Wu Wei
Publication year - 2007
Publication title -
liver international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.873
H-Index - 110
eISSN - 1478-3231
pISSN - 1478-3223
DOI - 10.1111/j.1478-3231.2007.01487.x
Subject(s) - calcitriol , calcitriol receptor , mapk/erk pathway , cell growth , cell culture , chemistry , hepatocyte growth factor , microbiology and biotechnology , apoptosis , cell cycle , cell , medicine , endocrinology , biology , receptor , vitamin d and neurology , kinase , biochemistry , genetics
Background: Previous studies have demonstrated that Calcitriol or its analogs has an anti‐tumour activity. This study was designed to determine the effect and mechanism of Calcitriol on MHCC‐97 heptocellular cell lines. Methods: MHCC97 cell lines were treated with Calcitriol of 10 −6 ∼10 −9 M concentration and with Calcitriol in lipiodol ultra‐fluid (LUF) respectively. The conditions of cell proliferation were analyzed by MTT method. The cell apoptosis and cycle were analyzed by using a flow cytometer. Hepatocyte growth factor (HGF) concentration in the cell supernatant was measured by using ELISA method. C‐met and vitamin D receptor (VDR) mRNA in cells were determined by using RT‐PCR method. VDR and ERK 1/2 proteins were determined by using Western Blotting method. Results: Calcitriol inhibited the proliferation of MHCC97 cell lines with an accumulation of cells in the G 0 /G 1 phase and reduction of cells in S phase. Calcitriol dissolved in LUF resulted in a better and longer inhibitive effect on the cell lines than Calcitriol alone. MHCC97 cell lines secreted HGF and expressed c‐met mRNA and ERK 1/2 proteins abundantly. Calcitriol remarkably inhibited the expressions of c‐met mRNA and ERK 1/2 proteins. Conclusion: Calcitriol inhibits the growth of MHCC‐97 heptocellular cell lines by down modulating c‐met and ERK expressions.